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*Ambient Particluate Matter Supresses Alveolar Macrophage Cytokine Response to Lipopolysaccharide
Citation:
Sawyer, K., M. C. MADDEN, AND A. J. GHIO. *Ambient Particluate Matter Supresses Alveolar Macrophage Cytokine Response to Lipopolysaccharide. Presented at Society of Toxicology Annual Meeting, Seattle, WA, March 16 - 20, 2008.
Impact/Purpose:
Diesel exhaust particles (DEP) suppress AM inflammatory cytokine response to lipopolysaccharide (LPS) from gram negative bacteria. We investigated if ambient PM induces similar suppression by exposing human AM in vitro to non-cytotoxic doses of Standard Reference Material (SRM) 2975 (DEP), SRM 1649 (urban dust), and North Carolina (NC) PM for 24 h.
Description:
Reports link ambient particulate matter (PM) exposure with cardiopulmonary mortality and morbidity, including the exacerbation of inflammatory disease and increased hospitalization for lung infections. Alveolar macrophages (AM) play an important defense role against infections via cytokine secretion. Diesel exhaust particles (DEP) suppress AM inflammatory cytokine response to lipopolysaccharide (LPS) from gram negative bacteria. We investigated if ambient PM induces similar suppression by exposing human AM in vitro to non-cytotoxic doses of Standard Reference Material (SRM) 2975 (DEP), SRM 1649 (urban dust), and North Carolina (NC) PM for 24 h. AM were then stimulated with LPS. 24-hr post LPS, DEP, Urban Dust, and NC PM suppressed extracellular IL-8 vs. unexposed AM. Increased intracellular IL-8 retention (50-70%) induced, in part, the decreased IL-8 release. 6 hr post LPS stimulation, DEP and NC PM significantly (p<0.05) suppressed total TNF-α (intracellular + extracellular) production from AM vs. unexposed AM. TNFα release also was suppressed in DEP-exposed AM incubated with lipotechoic acid (from gram+ bacteria), but not altered with phorbol ester or calcium ionophore stimulation. Our data suggested that mechanisms of TNFα release are dissimilar among these stimulants. Ambient PM modulated AM response to LPS. PM exposure may increase susceptibility to lung infection. PM components responsible for cytokine suppression are being examined as well as whether different PM induce unique lipid “fingerprints” that may explain AM responses. (Support: NHEERL-DESE Coop. Train. in Env Sci. Research, EPA CT826513. This abstract may not represent official EPA policy)